Ordered representations of the craniofacial periphery in the brain are necessary for normal sensory and motor functions of the face and head. While considerable experimental attention has been paid to the development and plasticity of central nervous system craniofacial representations, we still do not understand how they are maintained throughout life. The overall aim of the proposed research is to understand the necessary conditions for maintenance of peripherally determined central patterns of neuronal cell bodies and processes in the rodent trigeminal (V) system. We recently showed that attenuation of axonal transport in the infraorbital nerve (ION) with vinblastine results in a loss of all central fibrissae-related patterns. This is the only postnatal manipulation other than ION transection that has ever been demonstrated to have this effect and it occurs even though V primary afferent neurons in vinblastine-treated nerve maintain qualitatively normal projections to the periphery and brainstem. Our working hypothesis is that two conditions are necessary for the preservation of vibrissae-related patterns in the V brainstem complex: arrangement of the central arbors of vibrissae-related V ganglion cells in a pattern corresponding to the vibrissae; and, delivery of a peripherally derived neurotrophic factor by these primary afferents to V brainstem neurons In this "model," the vibrissae-related patterning of central ION axons provides correspondingly patterned concentrations gradients of the trophic factor which, in turn, result in the maintained aggregation of brainstem neurons. The patterning of cells in V nucleus principalis is required for the development and maintenance of corresponding vibrissae-related patterns in thalamus and cortex. While any of several neurotrophins might support the maintenance of central V patterns following transection of, or application of vinblastine to, the developing ION: 1) These manipulations cause a loss of central patterns secondary to the death of V ganglion and brainstem cells. 2) Central pattern loss results from lesion-induced abnormal functional input to the developing brainstem cells. 2) Central pattern loss results from lesion-induced abnormal functional input to the developing V brainstem complex. 3) The dramatic up-regulation of specific peptides (galanin and neuropeptide Y0 in input to the developing brainstem complex. Y) in surviving V ganglion cells and their central axons contribute to the loss of central vibrissae-related patterns after attenuation of axoplasmic transport or damage to, the ION. The experiments in this application will test our working hypothesis as well as these other possibilities regarding the mechanisms underlying the loss of central V patterns after application of vinblastine to the ION in newborn rats.